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Human TXNRD1 ELISA Kit for Sandwich ELISA - ABIN2685846
Mustacich, Powis: Thioredoxin reductase. in The Biochemical journal 2000
Show all 3 Pubmed References
NTRC is highly sensitive to rapidly changing light intensities.NTRC is not responsible for 'metabolism-related' regulation of the ATP synthase.
cooperative control of chloroplast functions via the FTR/Trx (show TXN ELISA Kits) and NTRC pathways is essential for plant viability
These data uncover a new role for NTRC in the control of photosynthetic yield.
An Arabidopsis thaliana double knockout mutant lacking NTRC and Srx (show SRX1 ELISA Kits) shows a phenotype similar to the ntrc mutant, while the srx (show SRX1 ELISA Kits) mutant resembles wild-type plants. NTRC deficiency causes reduced overoxidation of 2-Cys (show DNAJC5 ELISA Kits) peroxiredoxins.
NADPH thioredoxin reductase C is involved in redox regulation of the Mg-chelatase I subunit in Arabidopsis thaliana chloroplasts
interaction of chloroplast 2-Cys (show DNAJC5 ELISA Kits) peroxiredoxin with NADPH (show NQO1 ELISA Kits)-thioredoxin reductase C (NTRC) and thioredoxin (show TXN ELISA Kits) x
The strongest reduction in ntrc growth occurred under photoperiods with nights longer than 14 h, whereas knockout of the NTRC gene did not alter the circadian-clock-controlled growth. Lack of NTRC modulated chloroplast reactive oxygen species metabolism.
heat shock-mediated holdase chaperone function of NTRC is responsible for the increased thermotolerance of Arabidopsis and the activity is significantly supported by NADPH
analysis of electron transfer pathways and dynamics of chloroplast NADPH-dependent thioredoxin reductase C (NTRC)
NADPH (show NQO1 ELISA Kits)-thioredoxin reductase C (NTRC), previously reported as exclusive to green tissues, is also expressed in nonphotosynthetic tissues of Arabidopsis thaliana.
Selenoprotein TRXR-1 and GSR-1 (show GSR ELISA Kits) are essential for removal of old cuticle during molting in Caenorhabditis elegans.
High TRXR1 expression is associated with oral squamous cell carcinoma.
Inhibition of thioredoxin reductase-1 by brevetoxin-2 is via the formation of a Michael adduct between selenocysteine and the alpha, beta-unsaturated aldehyde moiety of the toxin.
Here, the authors use a novel assay to demonstrate that the reduction in non-native disulfides requires NADPH (show NQO1 ELISA Kits) as the ultimate electron donor, and a robust cytosolic thioredoxin (show TXN ELISA Kits) system, driven by thioredoxin reductase 1 (TrxR1 or TXNRD1).
Taken together, these findings indicate that auranofin inhibition of TrxR activity in Hep3B cells activates ROS (show ROS1 ELISA Kits)- and caspase (show CASP3 ELISA Kits)-dependent apoptotic signaling pathways and triggers cancer cell death.
It was observed that the combination of redox/protonation states of the N-terminal (FAD (show BRCA2 ELISA Kits) and Cys59/64) and C-terminal (Cys497/Selenocysteine498) redox centers defines the preferred relative positions and allows for the flexible arm to work as the desired electron "shuttle."
Our results clearly demonstrate that DIMC can synergistically enhance the cancer cell killing when combined with radiation by targeting thioredoxin (show TXN ELISA Kits) system.
thioredoxin reductase is inhibited by plumbagin, which leads to apoptosis in HL-60 cells
TXNRD1 variants may favor anti-tuberculosis drug-induced hepatotoxicity susceptibility in females and nonsmokers.
Our findings demonstrate that elevated TrxR1 levels correlate with the acquisition of bortezomib resistance in MM. We propose considering TrxR1-inhibiting drugs, such as auranofin, either for single agent or combination therapy to circumvent bortezomib-resistance and improve survival outcomes of MM patients.
Cardamonin exposure and selenium availability regulate expression of HO-1 (show HMOX1 ELISA Kits), GPX2 (show GPX2 ELISA Kits) and TrxR1 in human intestinal cells.
The developmental expression of cytosolic glutathione peroxidase (show GPX1 ELISA Kits) and TRXR1 during fetal development and the effect of maternal selenium consumption on the expression of these proteins are reported.
regenerated coronary endothelial cells exhibit downregulation of thioredoxin reductase
These results suggest that thioredoxin reductase (show PRDX5 ELISA Kits) may act as a positive regulator of NF-kappa B (show NFKB1 ELISA Kits) and may play an important role in the cellular inflammatory response.
data provide evidence for the involvement of the Trx/TrxR (show GSR ELISA Kits) system, in the regulation of haem oxygenase-1 expression in aortic endothelial cells during pro-oxidant challenge
GSR (show GSR ELISA Kits) is not essential for the maintenance of antioxidant defenses in mouse cochlea; the thioredoxin/thioredoxin (show TXN ELISA Kits) reductase (show PRDX2 ELISA Kits) system can probably operate as a functional backup for GSR (show GSR ELISA Kits).
TrxR1 represents a novel therapeutic target to prevent oxygen-mediated neonatal lung injury through Nrf2 (show NFE2L2 ELISA Kits).
The results demonstrate that DATS protects against oxidative stress-induced (show SQSTM1 ELISA Kits) DNA damage and apoptosis in C2C12 cells in part through the activation of Nrf2 (show NFE2L2 ELISA Kits)-mediated TrxR1 induction via the ERK (show EPHB2 ELISA Kits) signaling pathway.
Collectively, our results suggest that MsrA (show MSR1 ELISA Kits) protects hepatocytes from APAP-induced cytotoxicity through the modulation of TXNRD1 expression.
the timely upregulation of Trx1 (show TXN ELISA Kits)/TrxR1 and the active control of intracellular redox status is critical for the survival of thymocytes during and short after positive selection.
Considering the variable expression levels of Sep15 and TR1 found within the human population, our results provide insights into new roles of selenoproteins in cancer
Data suggest TXNRD1 and TXRNRD2 function at the top of a redox pyramid that governs the oxidation state of peroxiredoxins and other protein factors, thereby dictating a hierarchy of phenotypic responses to oxidative insults.
Augmentation of GSH systems by TrxR1 inhibition could represent a promising therapeutic approach to attenuate oxidant-mediated lung injury and improve patient outcomes.
Because the N-terminal domain of Sepp1 (show SEPP1 ELISA Kits) has a thioredoxin (show TXN ELISA Kits) fold, Sepp1 (show SEPP1 ELISA Kits)(UF) were compared with full-length Sepp1 (show SEPP1 ELISA Kits), Sepp1 (show SEPP1 ELISA Kits)(Delta240-361), and Sepp1 (show SEPP1 ELISA Kits)(U40S) as a substrate of thioredoxin reductase-1 (TrxR1).
Sec-containing TrxR1 is absolutely required for self-sufficient growth of MEFs under high-glucose conditions, owing to an essential importance of this enzyme for elimination of glucose-derived H2O2.
This gene encodes a member of the family of pyridine nucleotide oxidoreductases. This protein reduces thioredoxins as well as other substrates, and plays a role in selenium metabolism and protection against oxidative stress. The functional enzyme is thought to be a homodimer which uses FAD as a cofactor. Each subunit contains a selenocysteine (Sec) residue which is required for catalytic activity. The selenocysteine is encoded by the UGA codon that normally signals translation termination. The 3' UTR of selenocysteine-containing genes have a common stem-loop structure, the sec insertion sequence (SECIS), that is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Alternative splicing results in several transcript variants encoding the same or different isoforms.
thioredoxin reductase 1, cytoplasmic
, thioredoxin reductase 3
, thioredoxin reductase 1
, thioredoxin reductase 1, cytoplasmic-like
, KM-102-derived reductase-like factor
, gene associated with retinoic and IFN-induced mortality 12 protein
, gene associated with retinoic and interferon-induced mortality 12 protein
, thioredoxin reductase GRIM-12
, thioredoxin reductase TR1
, redox enzyme thioredoxin reductase
, NADPH-dependent thioredoxin reductase
, selenoprotein oxidoreductase
, TR alpha